Viruses are established as the causative agents in several types of malignancies in laboratory animals. It is clear that other factors, such as exposure to certain chemical agents, contribute significantly to the induction of tumors; it is generally accepted that malignant conversion by a variety of agents may have features in common. Understanding such common features as well as those uniquely related to a specific agent (or factor) should provide a basis for more informed treatment and control of malignant cells. A currently accepted model which accounts for neoplastic conversion by viruses suggests that viral DNA recombines with chromosomal DNA and alters genetic expression of the latter in daughter transformed cells. Our long range objective is the development of knowledge concerning the mechanism of the presumed recombination and malignant transformation. Our studies are also directed to understand the location and function of viral genes involved in the conversion to malignancy. The experimental approaches we use are aimed at extablishing in vivo parameter governing recombination. Some immediate objectives of these studies include fine mapping of the adenovirus 2 genome and the definition of host genes which function in viral malignant transformation. Biochemical, genetic and physical experiments are proposed and defined which should aid in understanding the functions of viral gene products in viral replication and viral oncogenesis.